doi.org/10.1590/S0004-2803.

230402023-64
REVIEW
The role of elastography in clinically
significant portal hypertension
Angelo Alves de MATTOS1,2, Angelo Zambam de MATTOS1,2,
Giovana Dal Pozzo SARTORI2, Gustavo Tovo BOTH³ and
Cristiane Valle TOVO1,2

1
Universidade Federal de Ciências da Saúde de Porto Alegre, Departamento de Clínica Médica,
Porto Alegre, RS, Brasil. 2 Universidade Federal de Ciências da Saúde de Porto Alegre, Curso de
Pós-Graduação em Medicina – Hepatologia, Porto Alegre, RS, Brasil. ³ Universidade Luterana do
Brasil, Departamento de Clínica Médica, Canoas, RS, Brasil.

HIGHLIGHTS ABSTRACT – This is a narrative review that aims to discuss the importance
• In compensated cirrhosis, using
non-invasive methods would exempt of elastographic methods in the evaluation of clinically significant
the patient from the need of an
endoscopy.
portal hypertension (CSPH) in cirrhotic patients, where the authors
propose an algorithm for evaluating these patients. In compensated
• The Baveno VII presented the
“rule of 5” for Vibration-Controlled advanced chronic liver disease, the goal is to prevent the develop-
Transient Elastography; liver stiffness
measurement ≤15 kPa and platelets ment of CSPH and, in those already with CSPH, prevent the appear-
>150.000/mm3 exclude clinically
significant portal hypertension ance of gastroesophageal varices (GEV) and other complications of
(CSPH), while when ≥25 kPa is
highly suggestive of CSPH. portal hypertension. In compensated cirrhosis, the prevalence of GEV
• Spleen stiffness measurement has is 30–40%, of which 10–20% are at risk of bleeding. Therefore, using
been proposed as a more specific
technique to predict the presence of non-invasive methods would exempt the patient from the need of an
CSPH.
endoscopy. Hepatic Elastography is a non-invasive, safe, reproduc-
• Elastography has gained prestige
in the non-invasive evaluation of ible method, available through many techniques: Vibration-Controlled
patients with advanced chronic liver
disease by allowing prophylactic
Transient Elastography (VCTE), Shear Wave Elastography (SWE) and
measures to be taken when Magnetic Resonance Elastography (MRE). The Baveno VII presented
suggesting the presence of CSPH.
the “rule of 5” for VCTE: liver stiffness measurement (LSM) ≤15 kPa
and platelets >150.000/mm3 exclude CSPH, while an LSM ≥25 kPa is
highly suggestive of CSPH. Also, the “rule of 4” for SWE has been
proposed: patients with ≥17 kPa could be considered as having CSPH.
Received: 24 April 2023
Accepted: 8 August 2023 At last, spleen stiffness measurement (SSM) has been proposed as a
more specific technique to predict the presence of CSPH. In conclu-
Declared conflict of interest of all
authors: none sion, elastography has gained prestige in the non-invasive evaluation
Disclosure of funding: no funding
received of patients with advanced chronic liver disease by allowing prophy-
Corresponding author: Cristiane
Valle Tovo. E-mail: lactic measures to be taken when suggesting the presence of CSPH.
cristianev@ufcspa.edu.br
Keywords – Portal hypertension; elastography; cirrhosis.

Arq Gastroenterol • 2023. v. 60 nº 4 • out/dez 525

Mattos AA, Mattos AZ, Sartori GP, Both GT, Tovo CV
The role of elastography in clinically significant portal hypertension
INTRODUCTION
When evaluating the burden of chronic liver dise-
ase(1), it is estimated that 1.5 billion patients are affec-
ted worldwide, with the most frequent causes being
non-alcoholic fatty liver disease (NAFLD), hepatitis B
and C viruses and alcoholic liver disease. Although
the number is probably underestimated, chronic liver
disease is responsible for 2.000.000 deaths per year
worldwide. In Brazil, liver disease is considered the
eighth most frequent cause of death(2).
Until recently, the diagnosis of chronic liver di-
sease was either histological, clinical, laboratory and
echographic or endoscopic in the case of advanced
disease. However, some tests are relatively invasive
and impractical for the constant follow-up of these
patients. This has raised interest in using non-inva-
sive methods for assessing patients with compensa-
ted cirrhosis, but these were not usually adopted in
clinical practice until very recently(3) Consequently,
elastography emerged as a robust and objective test
for diagnosing or excluding severe fibrosis/cirrhosis
and clinically significant portal hypertension (CSPH)
in cirrhotic patients. Accordingly, the Baveno VI and
Baveno VII consensus conference on portal hyper-
tension suggested that liver stiffness measurement
(LSM) can be used to identify patients having com-
pensated advanced chronic liver disease (cACLD)
and CSPH(4,5).
This is a narrative review that aims to discuss the
importance of elastographic methods in the evalua-
tion of CSPH in cirrhotic patients, especially hepatic
and splenic elastography, where the authors, in addi-
tion to reviewing the state of the art on the subject,
propose an algorithm for evaluating these patients.
Classification of cirrhosis
Six stages of cirrhosis must be considered when
classifying the disease(6). In stage 0, there is com-
pensated disease without CSPH. This stage is defi-
ned by a hepatic venous pressure gradient (HVPG)
between 5 and 10 mmHg and reasonable response
to the etiological treatment; in stage 1, the disease
remains compensated, however with CSPH (HVPG
≥10 mmHg) and, therefore, with a higher risk of de-
veloping varicose veins, hepatocellular carcinoma
and decompensation. In stage 2, the appearance of
526 Arq Gastroenterol • 2023. v. 60 nº 4 • out/dez
gastroesophageal varices (GEV) becomes evident,
and the 5-year mortality is about 10% if there is no
decompensation. In stage 3, bleeding due to variceal
rupture is already observed, with an estimated 5-year
mortality of 20% if there is no decompensation of
the liver disease. In stage 4, liver decompensation is
present (bleeding not included, as it is more often
related to the presence of ascites), with a 5-year mor-
tality of 55–80%; in stage 5, there are further episodes
of decompensation with a mortality up to 90% in 5
years. Finally, in stage 6, the patient has advanced
decompensated cirrhosis (refractory ascites, infec-
tion, persistent hepatic encephalopathy (HE), jaundi-
ce and renal dysfunction), with a high mortality rate
of 60 to 80% in 1 year.
Variceal veins are present in up to 40% of patients
with compensated cirrhosis (Child A) and up to 85%
in the decompensated (Child C)(7). In a study carried
out in our center evaluating a cohort of patients with
chronic liver disease on an outpatient basis, digestive
bleeding was the second most frequent complication
at the presentation for these patients(8). We emphasi-
ze that the recurrence of bleeding in one year could
be up to 60% and that the actual mortality of each
bleeding episode varies from 15 to 20%(7).
Screening for gastroesophageal varices in
cirrhosis
The screening criteria for GEV were based exclu-
sively on performing an upper digestive endoscopy
at the time of diagnosis of cirrhosis until a few years
ago. In 2015, the Baveno VI consensus(4) recommen-
ded that a measurement of less than 20 kPa when
performing Fibroscan®, associated with platelets
count greater than 150.000/mm3, would exempt the
patient from the need of an endoscopy. In the same
year, the European Association for the Study of the
Liver (EASL) guideline evaluating non-invasive tests
in liver diseases(9) considered that they should not
replace endoscopy to detect the presence of varicose
veins. Subsequently, many authors endorsed the po-
sition of Baveno VI(3,10), including the guidance from
the American Association for the Study of Liver Dise-
ases (AASLD)(11) that reiterated the recommendation
and suggested that when the possibility of high-risk
bleeding varices (HRBV) is low, non-invasive tests
could avoid the performance of a substantial num-

ber of endoscopies. However, international scientific
societies, including the EASL(12), emphasize that, be-
cause of the high risk of GEV in patients with decom-
pensated disease, endoscopy should be performed
annually in these patients.
Although we still consider endoscopy as an im-
portant screening tool in our center(13), we have in
mind that in compensated disease, the prevalence
of GEV is 30–40%, of which only 10–20% are at risk
of bleeding; therefore using non-invasive methods
would be advantageous. Since the data are negative,
the chance of HRBV is less than 5%, and up to 30%
of endoscopies would be avoided(14).
Changing paradigm in the assessment of patients
with cirrhosis and portal hypertension
As we can observe in the classification of cirrho-
sis(6), the prognosis of the disease begins to com-
promise the patient’s survival more significantly
from stage 3, when bleeding due to rupture of GEV
happens. Still, it becomes more evident in stage 4
(first episode of decompensation), when mortality
significantly increases. Thus, the premise should be
to avoid bleeding and other complications in patients
with cirrhosis, with CSPH being the leading cause of
these complications.
In cACLD without CSPH, when elastography does
not indicate CSPH (stage 0), the goal to be considered
is to prevent the development of CSPH by treating
or ruling out the cause of liver disease. In those al-
ready with CSPH (stage 1), the aim is to prevent the
appearance of GEV and other complications of portal
hypertension (ascites, HE). For this purpose, when
yet to be performed, it is necessary to treat the cause
of cirrhosis and adapt the patient’s lifestyle. However,
in many cases, even after successful treatment, CSPH
could persist(15), which leads us to infer that other me-
asures are necessary since this seems to be the marker
of hepatic decompensation episodes. In this way, the
treatment with medications acting specifically by lo-
wering portal pressure (NSBB) must be started(16).
More recently, when the role of hyperdynamic cir-
culation in cirrhosis and the response to NSBB were
re-evaluated, it was shown that patients without CSPH
have less hyperdynamic circulation and less reduction
in portal hypertension with the use of NSBB when
compared to those patients with CSPH(17). Based on
Mattos AA, Mattos AZ, Sartori GP, Both GT, Tovo CV
The role of elastography in clinically significant portal hypertension
this premise, the PREDESCI study(18) was designed,
which evaluated the role of NSBB in patients with
CSPH. This randomized, prospective, controlled, mul-
ticenter, double-blind study was conducted in patients
with compensated cirrhosis and CSPH. Patients who
responded acutely to NSBB were then randomized
into propranolol vs placebo and those who had not
responded to carvedilol vs placebo. The group that
used pharmacological therapy showed a better evo-
lution, and the authors concluded that NSBB increase
decompensation-free survival (exalting the role of lo-
wer incidence of ascites). This study was a milestone
in the treatment of patients with cirrhosis. From then
on, when faced with a patient with cACLD, the fo-
cus must be on the treatment of CSPH and no longer
punctually on the treatment of GEV.
The main studies that promoted a change in me-
dical management and those that established the
cut-off values for the non-invasive evaluation of
CSPH can be seen in TABLE 1.
The reduction in portal pressure improves the
evolution of cirrhosis in the presence or absence of
ascites, as demonstrated in a recent meta-analysis
with more than 1100 patients(20). When evaluating
primary prophylaxis, around half of the patients who
responded to NSBB, in addition to having less ble-
eding due to variceal rupture, had fewer complica-
tions related to cirrhosis decompensation, less need
for liver transplantation and lower mortality.
Despite the lack of head-to-head comparative stu-
dies between the two main NSBB available in our
country (propranolol vs carvedilol), there is a greater
tendency to use carvedilol, as it is believed to have
a more significant role in lowering the HVPG(21). The
use of carvedilol increases the proportion of respon-
ders to 75% vs 50% of other conventional NSBB(22).
In a systematic review and meta-analysis evaluating
four randomized controlled trials with 352 patients with
compensated cirrhosis and CSPH (without previous
bleeding), carvedilol decreased the risk of decompen-
sation and patient mortality(23). These data were corro-
borated in a recent study in an American cohort after 3
years of follow-up evaluating cirrhotic Child-A patients
with platelets between 30.000 and 150.000/mm3 and
no previous history of decompensation(24).
The consensus of Baveno VII(5), when taking a
position regarding the prevention of the first decom-
Arq Gastroenterol • 2023. v. 60 nº 4 • out/dez 527
Mattos AA, Mattos AZ, Sartori GP, Both GT, Tovo CV
The role of elastography in clinically significant portal hypertension

TABLE 1. Summary of data from studies on the evaluation of portal hypertension in cirrhotic patients.
Author
Groszmann RJ, et al.(19)
Villanueva C, et al.(17)
Villanueva C, et al.(18)
Albrades JC, et al.(3)
Pons M, et al. (43)
Rabiee A, et al.(45)
NSBB: non-selective ß-blockers; PH: portal hypertension; CSPH: clinical significant portal hypertension; RCT: randomized controlled trial; HRBV: high-risk
bleeding varices; cACLD: compensated advanced chronic liver disease; LSM: liver stiffness measurement; HCV: hepatitis C vírus; NASH: non-alcoholic
steatohepatitis; HBV: hepatitis B virus; AUC: area under the curve; VCTE: vibration-controlled transient elastography.
Design/N
Prospective N=213 cirrhotic
patients without varices
receiving timolol (n=108) vs
placebo (n=105)
Prospective, multicentric,
cross-sectional study N=273
cirrhotic with PH (194 with
CSPH and 79 with subclinical
PH)
Multicentric prospective,
double-blind, RCT
(PREDESCI). N=201 with
compensated cirrhosis and
CSPH without HRBV (100
received propranolol or
carvedilol and 101 received
placebo)
Prospective, multicentric
N=518 patients with cACLD
International cohort study
N=836 compensated cirrhotic
(358 HCV; 248 NASH; 203
alcohol abuse and 27 HBV)
Validation study N=245
patients with compensated
NASH cirrhosis
Aim/primary endpoint Results/conclusion
NSBB are ineffective in preventing varices/
Development of
bleeding (39% treated vs 40% placebo;
gastroesophageal varices
P=0.89) and are associated with adverse
or variceal hemorrhage
events
Patients with subclinical PH have less
To characterize the
hyperdynamic circulation and lower
hemodynamic profile
portal pressure reduction using NSBB
of each stage of PH in
compared to those with CSPH, suggesting
compensated cirrhosis
that NSBB are more suitable to prevent
and the response to NSBB
decompensation of cirrhosis in patients with
according to stage
CSPH than in earlier stages
Decompensation occurred in 16/100
(16%) patients in the NSBB group versus
NSBB to prevent 27/101 (27%) patients in the placebo
decompensation of group (P=0.041). Long-term treatment with
cirrhosis with PH NSBB could increase decompensation-
free survival in patients with compensated
cirrhosis and CSPH
To develop noninvasive Platelets ≥150.000 and a LSM value of 20
tests-based risk prediction kPa would have a predictive probability
models to provide a point- for HRBV of 5%, and 30% of the patients
of-care risk assessment of showed a predictive probability of HRBV
cACLD patients below 5%
To explore the prevalence
of PH in the most common
LSM ≥25 kPa is sufficient to rule in CSPH in
etiologies of patients
most etiologies, including non-obese with
with cACLD and develop
NASH, but not in obese patients with NASH.
classification rules based
LSM ≤15 kPa plus platelets ≥150.000 ruled
on LSM, that could be
out CSPH in most etiologies
readily used to diagnose or
exclude CSPH
To validate the ANTICIPATE
The ANTICIPATE models performed well in
models using baseline
predicting the presence of CSPH in NASH
data from a multicenter
cirrhosis. A model using FIB-4 plus albumin
RCT; and to develop and
(FIB4+) can be used to predict CSPH when
validate a model using
VCTE is not available
laboratory values (FIB4+)

pensation in patients with CSPH, suggests the use
of NSBB, giving priority to carvedilol as it is more
effective in reducing HVPG and in preventing de-
compensation, it decreases mortality, and it is better
tolerated. It reiterates that patients with NSBB and
cACLD do not need to undergo screening endoscopy
and recommends endoscopic band ligation in those
patients with HRBV with contraindication/intoleran-
ce to these drugs.
Thus, the new reality may be to focus more on
CSPH and less on the presence of GEV. The treat-
ment of the underlying disease and the use of NSBB
are the therapies to be used for this purpose, and
soon, the addition of new tools that could act at the
level of portal pressure, such as statins, could com-
plement the current therapeutic options.
Based on emerging data, the paradigm has shifted,
focusing on treating CSPH rather than just HRBV and
preventing any decompensation (variceal bleeding,
ascites, or HE)(25). Thus, returning to the classification
of cirrhosis(6), we would already start clinically inter-
vening in stage 1 (presence of CSPH without GEV)
and no longer in stage 2. However, CSPH is defined
by an HVPG ≥10 mmHg, and to confirm this diagno-
sis, we would have to perform an invasive procedure
that is not available in all medical centers. This could
lead to an impasse, but we believe that, over the
years, the evidence has grown to endorse the role
of non-invasive methods for diagnosing CSPH, even
though the gold standard remains the HVPG. Among
these methods, hepatic elastography has gained gre-
at prestige in literature.

528 Arq Gastroenterol • 2023. v. 60 nº 4 • out/dez


Hepatic elastography
Hepatic elastography is a non-invasive, safe, repro-
ducible method with good accuracy in evaluating li-
ver fibrosis. The mechanical changes that occur in the
liver as a result of liver fibrosis, promote an increase
in the organ’s resistance. Elastographic methods were
the standard for assessing the biomechanical proper-
ties of tissue(26,27). Thus, shear waves (SW) are gene-
rated when a directional force is applied to a tissue.
The ultrasound elastography consists of the LSM
through the evaluation of the speed of the shear wa-
ves, which can be mechanically produced by an ex-
ternal stimulus as the vibration-controlled transient
elastography - VCTE, used in the transient hepatic
elastography - Fibroscan® or through ultrasonic pul-
ses present in the shear wave methods like point
shear wave (p-SW) and two-dimensional shear wave
(2D-SW)(28-31). In the same way, magnetic resonance
elastography (MRE) also uses external stimuli(29,30).
The first and most validated technique is the VCTE:
a specific probe produces a vibratory wave into a
right intercostal space over the liver area, which is
transmitted to the liver. The result is expressed in
kilopascals (kPa). In this method, the operator has
little control over the evaluated area of interest, and
the image is one-dimensional(32). Newer methods
emerged, in which shear waves are produced by the
acoustic impulse of the ultrasound beam directly into
the liver, being called acoustic radiation force impul-
se (ARFI) techniques, generating shots in a single
point (pSWE) or in larger portions of the area of in-
terest to be evaluated (2D-SWE). All these latter te-
chniques allow real-time visualization of the area of
interest, with the result expressed in m/s or kPa(26,33).
VCTE is a one-dimensional technique that uses
elastic SW (50 Hz) and low-frequency ultrasound pro-
pagating through the skin and subcutaneous tissue
to the liver, performed with the FibroScan® system
(Echosens, France). The speed of the SW is directly
related to the stiffness of the tissue(34), which means
that the more resistant the tissue is, the faster the
manipulation of vibrations. VCTE is easy to perform,
reproducible, fast (takes 5–10 minutes) and can be
performed at the bedside or in an outpatient setting.
The results, expressed in kPa, and ranging from 1.5
to 75 kPa, are immediately available. It is a method
with high intra and interobserver agreement. Howe-
Mattos AA, Mattos AZ, Sartori GP, Both GT, Tovo CV
The role of elastography in clinically significant portal hypertension
ver, interobserver agreement becomes significantly
lower in patients with a body mass index (BMI) ≥25
kg/m², with steatosis in ≥25% of hepatocytes, hepatic
fibrosis <2 (METAVIR score), and in individuals with
narrow intercostal spaces(35).
The p-SWE was the pioneer in the inclusion of
a specific software coupled to the traditional ultra-
sound device to perform elastography. The B-mode
projected image on the screen allows the visualiza-
tion of the organ and the choice of the region of in-
terest (ROI) to acquire the speed of the shear waves.
Short-term acoustic pulses are emitted through the
transducer, generating SW at the ROI chosen by the
operator. Ultrasonographic images are used to guide
the placement of the ROI, and measurement is feasi-
ble even if ascites is present(26). The result will be the
median of 10 measures, and the reliability of the re-
sult is obtained with an interquartile range - IQR/me-
dian below 15%; the lower the IQR, the greater the
reliability of the test result. The pSWE has excellent
intra- and interoperator reproducibility for evaluating
liver elastography in healthy individuals and patients
with chronic liver disease(26).
The 2D-SWE follows the same principles described
for p-SW but with the ability to produce quantitative
SW images at a higher ROI and focus on multiple lo-
cations, sequentially detecting the time of arrival of the
SW in multiple lateral areas of the liver parenchyma(26).
The MRE has been highlighted in the non-invasi-
ve evaluation of liver fibrosis. The detection and sta-
ging of liver fibrosis is the main clinical application
of MRE, and it has been considered the most accu-
rate non-invasive method for detecting and staging
liver fibrosis, with excellent intra- and interobserver
agreement(36). Compared to other methods, it is the
only non-invasive technique capable of diagnosing
mild liver fibrosis with reasonable accuracy(37).
Factors that may influence the performance of the
methods
It must be emphasized that confounding bias,
such as inflammation (aminotransferases above five
times the upper limit of normal), liver congestion,
mechanic cholestasis, heart failure, biliary obstruc-
tion, as well as food intake, should be excluded due
to the misinterpretation of the results, mainly when
using VCTE and SWE(38).
Arq Gastroenterol • 2023. v. 60 nº 4 • out/dez 529
Mattos AA, Mattos AZ, Sartori GP, Both GT, Tovo CV
The role of elastography in clinically significant portal hypertension
Although most studies used VCTE as a reference,
studies using p-SWE or 2-D SWE almost always pro-
duced similar effects, suggesting that the same con-
founders must affect all techniques. For patients with
falsely elevated liver elastography measurements due
to alcoholic hepatitis, liver stiffness decreases after
1–4 weeks of abstinence. Other diseases that incre-
ase liver stiffness, independent of hepatic fibrosis,
include amyloidosis, lymphomas, and extramedulla-
ry hematopoiesis(26,28,39). Hepatic steatosis also causes
attenuation of the ARFI pulse and may lead to greater
variability in measurements(26).
Magnetic resonance imaging has been recognized
for decades as an important imaging method for the
liver. Although conventional anatomical images pro-
vide helpful diagnostic information, they have a limi-
ted role in diagnosing early-stage liver fibrosis and
cACLD(40). Park et al. performed a prospective study
comparing MRE vs VCTE’s performance for fibrosis
diagnosis in patients with NAFLD. A cross-sectional
study of 104 consecutive adults who underwent
MRE, VCTE, and liver biopsy was performed. The
authors found MRE to be more accurate than VCTE
in identifying liver fibrosis (stage 1 or more)(41).
For the diagnosis of cirrhosis in adults with NA-
FLD, the American Association of Gastroenterolo-
gy (AGA) reported that the use of the MRE is more
advantageous than the VCTE in a scenario of high
prevalence of cirrhosis, as it presents fewer false-
-positive results, reducing the number of patients un-
dergoing liver biopsy(42). The possibility of evaluating
a large sample volume, with the potential to assess
the entire liver volume, is recognized as one of the
main advantages of MRE compared to other metho-
ds for staging liver fibrosis. This characteristic is a
great advantage in staging since fibrosis often has
a heterogeneous distribution. Comparatively, biopsy
covers about 1/50.000 of the liver volume, and VCTE
covers about 1/100(36).
The main limitations of MRE include low availa-
bility, high cost, failures due to hepatic iron overload
and some general contraindications for performing
magnetic resonance. In addition, rigidity cut-offs
for different etiologies have yet to be established(36).
MRE is the most accurate non-invasive method for
detecting and staging liver fibrosis, especially in obe-
se patients with ascites.
530 Arq Gastroenterol • 2023. v. 60 nº 4 • out/dez
Hepatic elastography in the diagnosis of CSPH
The non-invasive diagnosis of CSPH in patients
with cACLD of different etiologies was recently eva-
luated in a cohort study with 836 patients with VCTE
paired with PVHG, where patients with LSM ≥10
kPa and without prior decompensation of liver di-
sease(43). Portal hypertension was observed in more
than 90% of cACLD patients, regardless of etiology,
except for patients with non-alcoholic steatohepatitis
- NASH (60.9%). In the latter population, this fact was
more evident in obese patients with NASH (53.3%).
When evaluating the presence of CSPH, the behavior
was similar, being also lower in patients with NASH
(50.5%), especially if obese (30.8%).
An LSM ≤15 kPa with platelet levels ≥150.000/
mm3 ruled out CSPH in most etiologies, while the
best cut-off point for determining CSPH in alcoholic
liver disease, chronic hepatitis B, chronic hepatitis C,
and patients with NASH was ≥25 kPa. In obese pa-
tients with NASH, the positive predictive value was
only 62.8%, so a nomogram was proposed to predict
CSPH in patients with NASH (ANTICIPATE-NASH),
where BMI was also considered(43).
Interestingly, the study demonstrates that decom-
pensation in advanced NAFLD can occur at lower
levels of PVHG(44). This study has the rationale that
the accuracy of PVHG in NAFLD may not reflect the
actual pressure of the portal vein. It is a multicenter
cross-sectional study of 548 patients with advanced
NAFLD versus 444 patients with cACLD caused by
hepatitis C virus. Median PVHG was lower in the
advanced NAFLD cohort (13 vs 15 mmHg), despi-
te similar liver function and higher rates of decom-
pensation in the advanced NAFLD cohort (32% vs
25%; P=0.019). The authors conclude that patients
with advanced NAFLD have a higher prevalence of
decompensation at any assessed portal hypertension
level (compared to those with advanced chronic liver
disease caused by the hepatitis C virus).
In the last Baveno meeting(5), the “rule of 5” was
presented. An LSM <10 kPa in the absence of clini-
cal or imaging events excludes compensated ACLD,
where there is a slight chance (<1%) of decompen-
sation or mortality. LSM between 10 and 15 kPa
suggests cACLD; LSM ≤15 kPa and platelets >150.000/
mm3 exclude CSPH (sensitivity and NPV >90%); LSM
≥15 kPa is highly suggestive of cACLD and LSM ≥25

kPa is highly suggestive of CSPH (specificity and PPV
>90%). In this scenario, there is a high risk of endos-
copic signs of portal hypertension and decompensa-
tion (less in obese patients with NAFLD). Although
in need of validation, the ANTICIPATE-NASH model
(LSM, platelets, BMI) can be used to predict the risk
of CSPH in patients with compensated NASH-cACLD.
More recently, a validation study confirmed that AN-
TICIPATE model performed well in predicting the
presence of CSPH in NASH cirrhosis and suggested a
new model using FIB-4 score plus albumin (FIB4+)
to predict CSPH where VCTE is not available(45).
Considering the cost of VCTE with Fibroscan®, it
is interesting to evaluate other non-invasive metho-
ds for diagnosing CSPH. Although most studies have
been conducted with the Fibroscan®, there could
also be space for ARFI techniques. In this regard,
an update of the consensus of the Society of Radio-
logists in Ultrasound Liver Elastography(31) proposed
the “rule of 4” in evaluating patients with cACLD,
including patients with viral etiology and NAFLD. In
this scenario, patients with ≥17 kPa (2.4 m/s) could
be considered as having CSPH. It does not mention
any difference in the use of p-SWE compared to 2D-
-SWE, although it points out that more studies are
needed for a more definitive answer regarding the
cut-off levels used in predicting the different stages
of the disease.
In the non-invasive detection of CSPH in cACLD,
Vuille-Lessard et al.(46) believe that p-SWE is not re-
commended to identify CSPH. However, considering
that the performance of 2D-SWE is probably consis-
tent with the VCTE, the heterogeneity of the cut-offs
(16 to 38 kPa) indicates a lack of standardization.
Although the method looks promising, more data is
awaited.
When monitoring patients with cACLD, an LSM
<20 kPa and platelets >150,000/mm3 would indicate
a low probability of HRBV, ruling out the need for
endoscopy. However, these patients must be follo-
wed annually with elastography. In patients with
contraindication/intolerance to NSBB, endoscopy
should be performed if LSM ≥20 kPa and platelets
<150.000/mm3(5).
Baveno VII suggests monitoring those patients
with LSM between 7–10 kPa and ongoing liver in-
jury. Decreased LSM correlates with a lower risk of
Mattos AA, Mattos AZ, Sartori GP, Both GT, Tovo CV
The role of elastography in clinically significant portal hypertension
decompensation and death (decrease ≥20% with LSM
<20 kPa or reduction to less than 10 kPa)(5).
Regarding the decrease of LSM, a study evalu-
ated non-invasive tests in diagnosing CSPH after
curing hepatitis C(47). They evaluated 418 patients
with PVHG ≥6 mmHg and sustained virological res-
ponse (SVR) who underwent post-treatment PVHG.
Three hundred twenty-four patients also had LSM/
platelet paired data. These patients were validated
for decompensation in 755 patients with SVR-cACLD.
In the PVHG/non-invasive testing cohort, for those
with cACLD, the pre/post-treatment prevalence of
CSPH was 80% and 54%, respectively. For certain
values of LSM/platelets, PVHG tended to be lower
post-treatment, indicating the need for specific algo-
rithms. The post-treatment LSM/platelet combination
produced high diagnostic accuracy in CSPH patients
with cACLD (AUC 0.884; 95%CI 0.843–0.926). A post-
-treatment LSM <12 kPa and platelets >150.000/ mm3
excluded CSPH (sensitivity: 99.2%), while an LSM
≥25 kPa was highly specific for CSPH (93.6%). In the
validation cohort, the 3-year risk of decompensation
was 0% in patients who met the criteria LSM <12
kPa and platelets >150.000/ mm3, whereas in patients
with post-treatment LSM ≥25 kPa, the risk of decom-
pensation was 9.6%. The authors conclude that non-
-invasive tests can estimate the likelihood of CSPH
after HCV cure and predict clinical outcomes. Thus,
patients with LSM <12 kPa and Platelets >150.000/
mm3 could be discharged from portal hypertension
surveillance if no cofactors are present, whereas tho-
se with LSM ≥25 kPa require surveillance/treatment.
In the consensus of Baveno VII(5), it is suggested
that after the removal/suppression of the etiological
factors in patients with cACLD, surveillance should
be carried out with the criteria of de Baveno VI, espe-
cially when the etiology of the liver disease is related
to hepatitis B and C viruses. After SVR, surveillance
is no longer necessary if LSM <12 kPa and platelets
>150.000/ mm3. In cACLD using NSBB without CSPH
after removal/suppression of etiological factors, en-
doscopy is recommended in 1-2 years and if there
are no GEV, suspension of NSBB is recommended(48).
Splenic elastography in the diagnosis of CSPH
Liver stiffness correlates with the severity of liver
fibrosis up to the threshold of CSPH(49). In patients
Arq Gastroenterol • 2023. v. 60 nº 4 • out/dez 531
Mattos AA, Mattos AZ, Sartori GP, Both GT, Tovo CV
The role of elastography in clinically significant portal hypertension
with CSPH, the strength of the correlation between
liver stiffness and fibrosis decreases, probably due to
an increasing role of extrahepatic factors, especially
the increase in portal venous inflow as portal hyper-
tension progresses(50). In this way, spleen stiffness
has been proposed as a more specific technique for
evaluating liver fibrosis in patients with CSPH. Ho-
wever, studies have yet to be performed to provide
reliable cut-off values(31).
It has been shown that splenic stiffness measure-
ment (SSM) is related to the progression of hepatic fi-
brosis, and in patients with hepatitis B or C infection,
SSM is increased even though the LMS is unchan-
ged(51,52). Subsequent studies have demonstrated that
SSM was positively correlated with HVPG and had
good performance in predicting CSPH and GEV in
cACLD patients(53,54). Also, it has been indicated that
although SSM is associated with portal hypertension,
it is insufficient to accurately assess its severity(55).
Further studies have suggested that SSM could relia-
bly rule out the presence of HRBV in cirrhotic pa-
tients independently of the etiology of cirrhosis(56,57).
In the same way, a recent systematic review and
meta-analysis evaluated the studies on the diagnos-
tic accuracy of SSM in detecting CSPH, severe portal
hypertension, GEV, and HRBV in patients with cA-
CLD. In this study, 32 studies (3.952 patients) were
identified, reporting the accuracy of SSM in diagno-
sing portal hypertension and/or GEV in adults with
cACLD. The results of this meta-analysis indicated
that SSM, by current techniques, had good accuracy
in detecting portal hypertension and GEV in cACLD
patients. AUCs for the diagnosis of CSPH exceeded
90%, and AUCs for any GEV and HRBV diagnosis
reached 87% and 83%, respectively. SSM was able
to predict the presence of CSPH with good sensi-
tivity and specificity (85% and 86%, respectively).
SSM was considered a promising method to detect
portal hypertension and GEV with good diagnostic
accuracy, and it would be a helpful non-invasive
surveillance tool for clinicians in managing cACLD
patients(58).
The acquisition technique is the same as that for
the liver, aside from the measurements being taken
between the left ribs with the patient in a supine or
slight right lateral position. Considering that signifi-
cant portal pressures are not expected at lower levels
532 Arq Gastroenterol • 2023. v. 60 nº 4 • out/dez
of fibrosis, SSM should only be taken in patients with
cACLD(31). It appears that SSM shows a better corre-
lation with portal pressure than LSM does(53). Portal
hypertension leads to splenic congestion, increasing
splenic stiffness, and it may even cause splenic fibro-
sis(59). In healthy individuals, the spleen is stiffer than
the liver. Several studies, most of which were perfor-
med with vibration-controlled transient elastography,
have shown that SSM is more reliable in patients with
portal hypertension than LSM for assessing the risk of
CSPH and esophageal varices(53,60,61). However, there
are differences in cut-off values between studies, and
the level of evidence is still too low to recommend
SSM in the diagnostic work-up of patients with cir-
rhosis(31). For ARFI-based techniques, limited studies
suggest that abdominal wall thickness and splenic
longitudinal diameter are independent predictors of
successful SSM(59). When using 2D SWE, it was de-
monstrated that CPSH is unlikely in patients with
SSM less than 26.6 kPa (3.0 m/sec)(62). Algorithms
that combine LSM and SSM, or platelets count, have
been proposed(63). In a multicenter study in which
LSM and SSM were available in 109 patients, this
algorithm had a sensitivity of 89.2% and a speci-
ficity of 91.4% to rule in CSPH(55). However, in a
series of 191 patients(64), this algorithm has not been
validated. The Baveno VII Consensus recommends
that SSM using VCTE can be used in cACLD due to
viral hepatitis to rule out and rule in CSPH (SSM
<21 kPa and SSM >50 kPa, respectively). Validation
of the best cut-off using a 100 Hz specific VCTE pro-
be, as well as using pSWE and 2D-SWE is needed.
Also, SSM ≤40 kPa by VCTE can be used to identify
subjects with a low probability of HRBV, in whom
endoscopy could be avoided(5).
The high failure rate (15–30%) observed with
SSM, mostly with VCTE and 2D-SWE, and the upper
measurement of 75 kPa (specific to VCTE) have
made SSM challenging to implement to this date.
Using the same probes and software for LSM may
not be appropriate, but SSM by VCTE has improved
significantly with the use of a spleen-dedicated VCTE
examination, where the SW frequency is set at 100
Hz instead of 50 Hz(46).
Given the data compiled in the literature(4,5,18,43),
we believe an algorithm can be recommended, as
shown in FIGURE 1.
 Mattos AA, Mattos AZ, Sartori GP, Both GT, Tovo CV
The role of elastography in clinically significant portal hypertension

FIGURE 1. Conduct in the prevention of CSPH in a patient with cACLD.

CSPH: clinical significant portal hypertension; cACLD: compensated advanced chronic liver disease; LSM: liver stiffness measurement.
FIGURE 1. Conduct in the prevention of CSPH in a patient with cACLD.
CSPH: clinical significant portal hypertension; cACLD: compensated
CONCLUSION dy; Mattos advanced
AZ, Sartori chronic
GP, Bothliver
GT, disease;
Mattos AALSM:
and:
liver stiffness measurement. Tovo CV contributed equally to drafting the article
It would be of interest to design studies evaluating and making critical revisions related to important in-
the evolutionary outcome of a liver disease contem- tellectual content of the manuscript. All authors have
plating the role of carvedilol vs placebo in patients read and approved the final version of the article to
with CSPH diagnosed by non-invasive tests. We have be published.
often used carvedilol in cirrhotic patients with signs
Orcid
TABLE of1:CSPH in the absence of contraindications. In those
Summary of data from studies on the evaluation of portal hypertension in cirrhotic
in which CSPH is only identified through non-invasi- Angelo Alves de Mattos: 0000-0003-2417-9765.
patients.ve methods (platelets and elastography), we suggest Angelo Zambam de Mattos: 0000-0002-3063-0199.
individualizing the use of the medication. Giovana Dal Pozzo Sartori: 0000-0002-2701-3499.
Author Design/N Aim/primary endpoint Results/conclusion
Gustavo Tovo Both: 0000-0003-4054-1242.
Groszmann RJ, etcontribution
Authors’ Prospective N=213 Cristiane ValleNSBB
Tovo:are
0000-0002-7932-5937.
(19)
ineffective in preventing
al. Mattos AA cirrhotic patients
and: Tovo CV without
conceptualized the stu-
Development of gastroesophageal varices/bleeding (39% treated vs 40%
varices receiving timolol
varices or variceal hemorrhage placebo; P=0.89) and are associated
(n=108) vs placebo
with adverse events
(n=105)
Villanueva C, et Patients with subclinical PH have less
(17)
al. hyperdynamic circulation and lower
Prospective, multicentric, To characterize the hemodynamic
portal pressure reduction using NSBB
cross-sectional study profile of each stage of PH in
compared to those with CSPH,
N=273 cirrhotic with PH compensated cirrhosis and the
suggesting that NSBB are more
(194 with CSPH and 79 response to NSBB according to
suitable to prevent decompensation of
with subclinical PH) stage
Arqcirrhosis in patients
Gastroenterol with
• 2023. v. 60 nº 4CSPH than
• out/dez 533in
earlier stages
Mattos AA, Mattos AZ, Sartori GP, Both GT, Tovo CV
The role of elastography in clinically significant portal hypertension

Mattos AA, Mattos AZ, Sartori GP, Both GT, Tovo CV. O papel da elastografia na hipertensão portal clinicamente significativa. Arq
gastroenterol. 2023;60(4):525-35.
RESUMO – Trata-se de uma revisão narrativa que visa discutir a importância dos métodos elastográficos na avaliação da hipertensão
portal clinicamente significativa (HPCS) em pacientes cirróticos, onde os autores propõem um algoritmo para avaliação desses pa-
cientes. Na doença hepática crônica avançada compensada, o objetivo é prevenir o desenvolvimento de HPCS, e naqueles já com
HPCS prevenir o aparecimento de varizes gastroesofágicas (VGE) e outras complicações da hipertensão portal. Na cirrose compen-
sada, a prevalência de VGE é de 30–40% e 10–20% são varizes com risco de sangramento, portanto o uso de métodos não invasivos
dispensaria o paciente de endoscopia. A elastografia hepática é um método não invasivo, seguro e reprodutível, disponível através
de várias técnicas: elastografia transitória (VCTE), onda de cisalhamento (SWE) e elastografia por ressonância magnética. O Baveno
VII apresentou a “regra dos 5” para VCTE: medida da rigidez hepática (LSM) ≤15 kPa e plaquetas >150.000/mm3 excluem HPCS
enquanto um LSM ≥25 kPa é altamente sugestivo de HPCS. Além disso, foi proposta a “regra dos 4” para SWE: pacientes com ≥17
kPa podem ser considerados como portadores de HPCS. Por fim, a medição da rigidez do baço (SSM) foi proposta como uma
técnica mais específica para prever a presença de HPCS. Em conclusão, a elastografia ganhou prestígio na avaliação não invasiva
de pacientes com doença hepática crônica avançada, ao permitir a adoção de medidas profiláticas ao sugerir a presença de HPCS.
Palavras-chave – Hipertensão portal; elastografia; cirrose.

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